The invention relates to vascular repair devices, and in particular intravascular stents, which are adapted to be implanted into a patient's body lumen, such as a blood vessel or coronary artery, to maintain the patency thereof. Stents are particularly useful in the treatment of atherosclerotic stenosis in arteries and blood vessels.
Stents are generally tubular-shaped devices which function to hold open a segment of a blood vessel or other body lumen such as a coronary artery. They also are suitable for use to support and hold back a dissected arterial lining that can occlude the fluid passageway. At present, there are numerous commercial stents being marketed throughout the world. For example, the prior art stents depicted in FIGS. 1-5 have multiple cylindrical rings connected by one or more undulating links. While some of these stents are flexible and have the appropriate radial rigidity needed to hold open a vessel or artery, there typically is a tradeoff between flexibility and radial strength and the ability to tightly compress or crimp the stent onto a catheter so that it does not move relative to the catheter or dislodge prematurely prior to controlled implantation in a vessel.
Presently, there is substantial development of drug coated stents, particularly in the coronary arteries, to reduce the likelihood of the development of restenosis after the stent has been implanted. One problem being encountered with stent, including these drug coated stents, is that restenosis can sometimes occur at the stent ends, both distally and proximally of the implanted stent. The development of restenosis at the stent ends is sometimes referred to as peri-stent restenosis. While various theories exist as to the reasons for the development of restenosis at the stent ends, one important factor appears to be injury to the arterial wall by the non-working length of the balloon. In other words, that portion of the balloon that extends beyond the stent will expand into the arterial wall and cause stretching or other injury that will eventually lead to the development of restenosis. The drug coating on the stent will release the drug substantially in the area where the stent contacts the arterial wall, leaving the distal and proximal areas beyond the stent untreated with the therapeutic drug. As a result, the likelihood of the development of restenosis beyond the ends of the stent is much greater since the therapeutic drug does not treat that injured area.